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      Advanced Oxidation Protein Products, Parathyroid Hormone and Vascular Calcification in Uremia

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          Vascular calcification is a frequent complication of uremic patients. In addition to classical risk factors such as age, male gender, smoking, inflammation, hypertension, dyslipidemia, and diabetes, which also exist in the general population, patients with chronic renal failure have other risk factors such as oxidative stress, inflammation, hyperparathyroidism, hypoparathyroidism, hypercalcemia, hyperphosphatemia, and overtreatment with calcium and vitamin D. These latter risk factors may even have a better predictive value than classical risk factors for coronary heart disease in uremic patients.

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          Morphological predictors of arterial remodeling in coronary atherosclerosis.

          Although arterial remodeling in atherosclerotic arteries affects luminal patency, the role of plaque components has not been systematically studied. Coronary segments (n=2885) were harvested from the hearts of 36 patients who died of severe coronary artery disease after perfusion fixation. Remodeling was determined by morphometric analysis of 657 sections selected as reference segments and 1318 segments with atheromatous plaques. Atherosclerotic plaques were identified as fibroatheroma, thin-cap fibroatheroma, intraplaque hemorrhage with or without rupture or erosion, or total occlusion. Plaque components consisted of calcification, lipid core, macrophage burden, and fibrosis. There was no correlation between plaque area and lumen size in proximal arteries, unlike middle and distal segments, which demonstrated a significant correlation. Marked expansion of the internal elastic lamina (IEL) occurred in plaque hemorrhages with or without and thin-cap fibroatheroma (vulnerable plaque), whereas in erosions and total occlusions there was shrinkage of the IEL. Macrophage burden, lipid core size, calcium (in fibrous plaque and lipid core), and medial atrophy were all associated with positive remodeling; fibrous areas, however, were negatively associated with remodeling. Inflammation, calcification, and medial thinning are primary determinants of positive remodeling, which appears to be a feature of plaque instability.
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            Monocyte/macrophage regulation of vascular calcification in vitro.

            Calcification is a common complication of atherosclerosis and other chronic inflammatory processes that involves infiltration of monocytes and accumulation of macrophages. To determine whether these cells modulate vascular calcification in vitro, calcifying vascular cells (CVCs), a subpopulation of osteoblast-like cells derived from the artery wall, were cocultured with human peripheral blood monocytes for 5 days. Results showed that alkaline phosphatase (ALP) activity, a marker of osteoblastic differentiation, was significantly greater in cocultures than in cultures of CVCs or monocytes alone. Both ALP activity and matrix mineralization increased in proportion to the number of monocytes added. Activation of monocyte/macrophages (M/Ms) by oxidized LDL further increased ALP activity in cocultures. However, neither conditioned medium from oxidized-LDL-activated M/Ms or transwell coculture had this effect on CVCs, which suggests a need for cell-to-cell contact. In contrast, conditioned medium from lipopolysaccharide-activated M/Ms increased ALP activity of CVCs. ELISA showed that lipopolysaccharide-activated M/Ms secreted tumor necrosis factor-alpha, and neutralizing antibody to tumor necrosis factor-alpha attenuated the induction of ALP activity by the conditioned media. These results suggest that M/Ms enhance in vitro vascular calcification via 2 independent mechanisms: cell-cell interaction and production of soluble factors such as tumor necrosis factor-alpha.
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              Medical Management of Secondary Hyperparathyroidism in Uremia


                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                30 August 2002
                : 20
                : 5
                : 494-497
                Inserm U507 et Service de Néphrologie, Hôpital Necker, Paris, France
                65203 Blood Purif 2002;20:494–497
                © 2002 S. Karger AG, Basel

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                References: 30, Pages: 4
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/65203


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